Hip and knee replacements are common and successful surgeries in orthopaedics. One of the known complications is fat embolism. Cemented implants used in arthroplasty allow good implant fixation and excellent long term results. However this has been associated with an increased incidence of fat embolism. This experimental animal study compared the amount of fat embolism following three different surgeries in 30 Sprague Dawley rats. These surgeries simulated hip replacement procedures and included a control surgery, an un-cemented implant and a cemented implant. These animals were then sacrificed at 24 hours. All the lungs were fixed in formalin and then stained using Osmium Tetroxide. The amount of fat was then counted using a light microscope at 40x power. Both the uncemented implant group (p < 0.001) and the cemented implant groups (p < 0.003) had significantly higher fat emboli from the surgical control group. There were also a significantly higher number of emboli (p < 0.05) in the cemented implant group compared to the uncemented implant group. We conclude that fat embolism occurs in both the un-cemented and cemented hip replacement. The amount of emboli created by un-cemented hip replacement is less than the cemented hip replacement. The cement itself does not cause the complication of fat embolism. It is the high intramedullary pressure associated with the insertion of the implant, and the cementing process, that contributes to fat embolism. Devices or surgery that minimise this rise in pressure could reduce the amount of fat embolism

The Pulmonary Embolism Prevention (PEP) Trial was designed to assess the effects of a 35 day course of aspirin (160 mg daily) on the risks of thromboembolic events, other cardiovascular outcomes and bleeding among individuals undergoing surgery for hip fracture or joint replacement. From 1992 to 1998, 148 hospitals in Australia, New Zealand, South Africa, Sweden and the United Kingdom randomised 13,356 hip fracture patients, and 22 hospitals in New Zealand randomised 4,088 elective arthroplasty patients. Among hip fracture patients, aspirin produced proportional reductions in PE of 43% (95% confidence interval [CI] 18% to 60%; 2P=0.002) and symptomatic DVT of 29% (95% CI 3% to 48%; 2P=0.03). PE or DVT was confirmed in 105 (1.6%) of 6679 patients allocated aspirin versus 165 (2.5%) of 6677 allocated placebo, representing an absolute reduction of 9±2 per 1000 and a proportional reduction of 36% (95% CI 19% to 50%; 2P=0.0003). Aspirin prevented 4±1 fatal pulmonary emboli per 1000 treated (18 aspirin vs 43 placebo deaths), representing a proportional reduction of 58% (95% CI 27% to 76%; 2P=0.002), with no apparent effect on deaths from other vascular (hazard ratio 1.04; 95% CI 0.86 to 1.26) or non-vascular cause (1.01; 95% CI 0.84 to 1.23). Deaths due to bleeding were rare (13 aspirin vs 15 placebo), but there was an excess of 6±3 post-operative transfused bleeds per 1000 allocated aspirin (2P=0.04). Among elective arthroplasty patients, venous thromboembolism rates were lower but the proportional effects of aspirin appeared similar to those among hip fracture patients

This study was undertaken to assess the contribution of pulmonary fat embolism to systemic platelet activation in a rabbit model of fat embolism. Fifteen NZW rabbits were randomly assigned into one of two groups: fat embolism and control. Fat embolism was induced via intramedullary canal pressurization with a 1–1.5 ml bone cement injection. Only the animals that underwent fat embolism displayed consistent platelet activation, as demonstrated by platelet degranulation and procoagulatory surface expression. These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma. The objective of this study was to use a recently developed rabbit model of fat embolism to assess the systemic hemostatic response to pulmonary fat embolism. Our findings demonstrate platelet activation following forced liberation of bone marrow contents into the circulation only in the FE group, as demonstrated by CD62P elevation (a marker of platelet degranulation) and annexin V elevation (a marker of procoagulatory surface expression). Platelet activation also coincided with significantly lower platelet counts in the FE group at two and four hours post embolism, suggesting platelet aggregation. These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma. Platelet count decreased significantly at two and four hours post knee manipulation only in the FE group. Annexin V expression increased significantly in the FE group at two and four hours post knee manipulation. Lastly, CD62P expression only increased significantly in the FE group at two hours post knee manipulation. Fifteen New Zealand White male rabbits were randomly assigned into one of two groups: control and fat embolism (FE). In FE group (n=8), the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. In the control group (n=7), a sham knee incision was made, exposing both femoral condyles, but was immediately closed without further manipulations. All animals were mechanically ventilated for an additional monitoring period of four hours post-surgical closure. For flow cytometric evaluation of platelet activation, blood samples were stained with fluorescence-conjugated antibodies against CD41 (FITC), CD62P (P-selectin) and annexin V (FITC). Platelet events were identified by their characteristic CD41 staining and size and were analyzed using a flow cytometer. All animals were mechanically ventilated for four hours post surgical closure. The implications of platelet activation following fat embolism are numerous, ranging from adherence and aggregation, to secretion of key components of both the coagulation and inflammatory cascades

This study was undertaken to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock and fat embolism, resuscitated hemorrhagic shock, fat embolism, and control. Fat embolism was induced via intramedullary cavity with a 1–1.5 ml bone cement injection. Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome. The objective of this study was to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome. CD11b mean channel florescence was only significantly elevated in the HR/FE group at two and four hours post knee manipulation. Moreover, greater infiltration of alveoli by leukocytes was only significantly higher in the HR/FE group as compared to controls. Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Hypovolemic shock was induced via carotid bleeding for one-hour prior to resuscitation. For fat embolism induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. For evaluation of neutrophil activation, blood was stained with antibodies against CD45 and CD11b and analyzed with a flow cytometer. Animals were mechanically ventilated for four hours post surgical closure. Postmortem thoracotomy was performed, and three stratified random blocks of each lung were processed for histological examination. Our findings suggest that FE by itself does not cause lung injury, as there were no apparent differences between the control and FE animals. Only the HR/FE animals revealed a higher number of infiltrating neutrophils into alveolar spaces and greater neutrophil activation

Introduction Cement leakage into adjacent structures is the main complication during vertebroplasty. The majority of these leaks are asymptomatic, but pulmonary cement embolism has been reported to cause cardiovascular disturbances and even death (. 1. ,. 2. ). Furthermore, the use of calcium phosphate (CaP) cements for vertebroplasty may aggravate cardiovascular deterioration in the event of cement embolism by stimulating coagulation [3]. The cardiovascular effects of pulmonary cement embolism were investigated using an animal model. Methods In 18 skeletally mature sheep, 2.0ml cement was injected into the pulmonary trunk during general anaesthesia (approved by Animal Ethics Committee). Three different cements were used: 1) PMMA (Simplex P, Stryker); 2) PMMA with 10% hydroxyapatite (PMMA & HA) (Vertecem, Synthes); 3) Experimental injectable CaP cement (Synthes). The following cardiovascular parameters were recorded continuously (endpoint: 60min post-injection): arterial, central venous, pulmonary arterial pressures and cardiac output. Blood gases and coagulation parameters (antithrombin, D-dimer, prothrombin fragments I & II) were measured pre-injection, 10, 30 and 60min post-injection. Postmortem, lungs were removed intact and submitted to computer tomography (CT) imaging. Results There were no fatalities. After 1min, mean pulmonary arterial pressure had increased by 9%, 14% and 21% from pre-injection value in the PMMA, PMMA & HA and CaP group respectively. Differences in pulmonary arterial pressure between the three material groups were not statistically significant. Pulmonary arterial pressure stayed elevated for the duration of the experiment (i.e. 60min post-injection). There were no other significant changes in cardiovascular, blood gas or coagulation parameters from pre- to post-injection values. Three dimensional reconstructions of the CT images showed a tendency of the CaP cement to break up into multiple smaller pieces whereas the two other cements did not. Discussion Cement embolism led to mild pulmonary hypertension in all material groups. Present results are in contrast to earlier reports (pig model) of fulminant cardiovascular deterioration after CaP cement embolism (. 3. ). Present changes were not as severe and there was no evidence of thromboembolism. This discrepancy may have been due to differences in the cement formulations or the animal model. Pulmonary hypertension was more severe in the CaP cement group. This may have been due to the disintegration of the CaP cement resulting in blockage of more pulmonary vessels compared to the PMMA cements

Background: Cerebral emboli may be detected by transcranial Doppler (TCD) in patients undergoing hip arthroplasty. Venous – arterial circulation shunts (v-aCS), cerebral embolism and postoperative organ dysfunction were investigated in elective hip arthroplasty. Methods: TCD was used to identify v-aCS in (i) elective hip arthroplasty (n=45), (ii) abdominal aortic aneurysm surgery (AAA) (n=20) and (iii) transurethral resection of prostate (TURP) (n=10). A v-aCS was diagnosed when 1 or more microbubbles were detected in the middle cerebral artery by TCD following intravenous injection of a microbubble emulsion. TCD was also used to monitor for intraoperative cerebral emboli (ICE). Cognitive function was measured by a battery of computerised tests before and 5 days after surgery. Troponin T, AST, ALP, Bilirubin, Creatinine, Urea and Creatinine clearance were measured pre-operatively and 24 and 48 hours post-operatively. Results: Cerebral embolism occurred in 26 of 45 patients during hip arthroplasty (median 4, range 1 – 368) but not during AAA or TURP surgery. Cerebral embolism only occurred in patients with a v-aCS (p< 0.001) and was strongly associated with the size of the v-aCS (rs=0.8, p< 0.001). The number of ICE had no influence on Troponin T, renal function, liver function or cognitive function. Conclusion: Cerebral embolism is common in patients with a v-aCS during hip arthroplasty. There was no evidence of cerebral or multi-organ damage due to paradoxical embolism

This study was undertaken to assess the contribution of fat embolism (FE) to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock and FE (HR/FE), resuscitated hemorrhagic shock, FE, and control. FE was induced via intramedullary femoral canal pressurization using a 1–1.5 ml bone cement injection. Only HR/FE animals displayed significant proinflammatory cytokine release as compared to controls. These findings suggest that the combination of resuscitated shock with FE initiates an inflammatory response, which may lead to the development of fat embolism syndrome. The objective of this study was to assess the contribution of fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Only the animals that underwent resuscitated shock and fat embolism displayed amplified BALF proinflammatory cytokine expression. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome. Only HR/FE BALF IL-8 and MCP-1 levels were significantly higher than controls (0.72 ng/ml vs. 0.26ng/ ml, p=0.03; 18.3 ng/ml vs. 2.0 ng/ml, p=0.01, respectively). Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Shock was induced via carotid bleeding for one-hour prior to resuscitation. For FE induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. Four hours later, postmortem bronchoalveolar lavage was performed through the right mainstem bronchus. Analyses of bronchoalveolar lavage fluid (BALF) of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were carried out in triplicate and blinded fashion using the ELISA technique. Our findings suggest that FE by itself does not initiate inflammatory lung injury, as there were no apparent differences between the control and FE cytokine levels. Only the HR/FE animals revealed elevated levels of pro-inflammatory cytokines in BALF. These findings are in agreement with our previous results, which displayed neutrophil activation only in the HR/FE group

Purpose: Fat or marrow embolism during or after bone and joint surgery is a serious complication. We wanted to determine the incidence and circumstances of peroperative embolism in patients undergoing lumbar spine surgery with and without instrumentation. Material and methods: Sixty adult patients with degenerative lumbar spines underwent peroperative and early postoperative transoesophageal ultrasonography. The lumbar procedure involved instrumentation with insertion of pedicular screws in 40 patients. Results: Moderate to severe signs of embolism (Pitto classification grade 2 or 3) were observed in 80% of the patients who underwent instrumentation procedures but in none of those who had not been instrumented (p < 0.001). Discussion: Among the different procedures performed on the posterior lumbar spine, insertion of pedicular screws appears to be the leading cause of pulmonary embolism. The approach, laminectomy, discectomy, and bone abrasion do not appear to produce detectable embolism. Conclusion: We consider that the observed embolic manifestations, also observed in intramedullar procedures, are potentially fatal after spinal surgery

Introduction. Pulmonary embolism (PE) complicates up to 1% of total joint arthroplasties (TJA). Many PE treatment guidelines call for immediate initiation of therapeutic anticoagulation. Options include Xa inhibitors, Enoxaparin, and Warfarin. Deciding between these is a balance of the efficacy and the risks. Little data exists regarding the risks of each of these treatment options for treating PE in arthroplasty patients. Methods. We examined the records of 29,270 patients who underwent a primary total joint arthroplasty (TJA), defined as a unilateral total knee arthroplasty (TKA) (18,987) or total hip arthroplasty (THA) (10,283), between 2/2016 and 12/2018 at our institution and identified 338 (242 TKA, 96 THA) patients who developed an in-hospital PE treated with therapeutic anticoagulation. The patients were treated with therapeutic doses of Xa inhibitors, enoxaparin or warfarin. The type and frequency of complications were determined and classified as major or minor. Major complication included: bleeding requiring surgery, GI bleed requiring treatment, >2 unit transfusion and mortality. Minor complications included wound drainage, bleeding not requiring surgery, and thrombocytopenia. Results. Overall complication rates were high for all treatments. Xa inhibitors had the lowest complication rate at 14% compared to 20% for enoxaparin and 20.7% for warfarin though the difference did not quite reach statistical significance (p=.054). Both major and minor complication were lower with Xa inhibitors, but again the difference was not statistically significant (p=0.67). There was no significant difference in complications between TKA groups (p=0.73) or THA groups (p=0.83). Gender and body mass index were not predictive of major or minor complications. Discussion. Our results demonstrate high complication rates associated with modern therapeutic anticoagulation protocols for perioperative PE following TJA. Patients who receive therapeutic anticoagulation postoperatively are at high risk for complication. Xa inhibitors may decrease these risks, but larger studies are required

Introduction. Total knee arthroplasty (TKA) is one of the most successful surgeries to relieve pain and dysfunction caused by severe arthritis. However, it is a still big problem that there is a possibility of death in pulmonary embolism (PE) after TKA. We previously reported that there was more incidence of asymptomatic PE than estimated in general by detail examinations. But it was difficult to whom we decided to perform additional examinations except the patients with some doubtful symptoms. Therefore, we investigated detail of PE patients after primary TKA to find out anything key point in PE. Methods. Consecutive ninety-nine patients who underwent primary TKA from January 2015 to March 2018 were applied. There were 23 male and 76 females included, and the mean age was 73.7 years old. There were 96 cases of osteoarthritis, 2 cases of osteonecrosis and one of rheumatoid arthritis. A single knee surgery team performed all operations with cemented type prostheses and air tourniquet during operation. There were 35 cases of one-staged bilateral TKA and 64 of unilateral TKA. Detail examinations with contrast enhanced CT (CE-CT) and venous ultrasonography (US) were performed at the 3rd day after surgery. Next, we applied ultra sound cardiogram (UCG) to the patients diagnosed as PE by CE-CT, we checked right ventricular overload (RVO) to treat PE. These images were read by a single senior radiologist team. Results. CE-CT was performed in 87 patients (87.8%) and US was in all patients. The incidence of deep vein thrombosis (DVT) was 67 patients (67.6%), and all of these was distal type DVT. PE was 17 patients (17.1%), and each of patients had no symptoms. RVO was detected in 5 patients (5.0%), and two of them (2.0%) had decreased SpO2 in early 90% perioperative period. All patients did not change rehabilitation protocol and progress was good until discharge. Conclusion. We investigated consecutive 99 patients for DVT/PE after primary TKA using CE-CT and venous US. And we performed UCG to PE patients. One of the important findings to decide detail examination for asymptomatic PE was decrease in SpO2 during early perioperative period. It might be the only finding except symptom. We also have to be more aware about high incidence of asymptomatic PE and more careful to the patients after TKA to prevent complications. For any figures or tables, please contact authors directly

Background. Orthopaedic surgeons are increasingly pressured to consider thromboprophylaxis for patients when little evidence exists. The aim of this study was to determine the incidence of fatal pulmonary embolism following office attendance in our outpatient fracture clinic. Methods. Between October 2004 and September 2006 details of all new patients referred to our orthopaedic fracture clinic were prospectively entered into an audit database. Patients did not receive any form of thromboprophylaxis. Data was cross referenced with a national mortality database to identify all patients who subsequently died within 90 days of attendance in fracture clinic. Results. 11,502 new patient fracture clinic appointments occurred during the study period. 5604 patients had lower limb injuries. Twenty three patients died within 90 days of being seen. The mean age of these patients was 75 years (range 52–100). Two of the 23 patients attended fracture clinic with lower limb injuries. Review of the medical records showed no evidence of pulmonary embolism. Assuming a worst case scenario that both died of fatal pulmonary embolism the incidence of fatal pulmonary embolism following attendance in fracture clinic with a lower limb injury is no higher than 0.036% (95% CI 0.09%–0.33%). Conclusion. The incidence of fatal PE following outpatient management of lower limb fractures is very low. This incidence data will inform decisions on the risk-benefit analyisis of thromboprophylaxis in this group of patients

Purpose: This study was designed to evaluate post-total joint arthroplasty patients who were sent for a chest CT scan in order to determine the clinical factors that were most likely to be associated with, and predictive of, a radiologic diagnosis of pulmonary embolism in the acute, postoperative period. Method: The current study involved a review of 540 total knee replacements and 543 total hip arthroplasty procedures performed from June 2008 to September 2009. All patients received postoperative VTE prophy-laxis using LMWH, as per the protocols established by the Alberta Bone and Joint Initiative, and consistent with the recommendations of the American College of Chest Physicians (2008). A pulmonary CT scan was ordered for patients in situations where. a pulmonary embolism was strongly suspected. for those who lacked a clear alternative diagnosis as an explanation for their findings. when steps to correct the suspected underlying condition failed to normalize results, or. in situations where the diagnosis (i.e. new-onset atrial fibrillation) warranted further investigation to rule out a PE as a possible cause. Patients referred for multidetector computed tomography to investigate the possibility of pulmonary embolus were identified, and subjected to a chart review. Results: Forty-two patients underwent a pulmonary CT scan investigation to rule out pulmonary embolus. Of these, 15 patients had undergone hip surgery, and 27 had undergone a total knee replacement. Of the 42 patients, 34 exhibited hypoxemia as their major presenting sign (oxygen saturation less than 90% on room air), with or without other signs or symptoms. Four patients presented with tachycardia alone, and 2 patients presented with chest pain, of which one patient had an associated arrhythmia. Of the 34 patients presenting with unexplained postoperative hypoxemia, 25 were patients who had undergone total knee replacement, and of these 25 patients, 14 (56%) were found to have a pulmonary embolus on CT scanning of the lungs. There were no PE’s identified in the post-hip population. None of the patients with PE’s presented with subjective dyspnea or chest pain. There were no fatalities as a result of PE. Conclusion: The overall high rate of detection of pulmonary embolism in our postoperative population is due the very close monitoring of pulse oximetry combined with the improved sensitivity of imaging modalities. Hypoxemia is emerging as the clinical sign that is most sensitive to the possibility of a PE in the post-knee arthroplasty patient. Reliance on clinical symptoms such as chest pain, dyspnea, or even tachycardia is no longer appropriate. It is recommended that oxygen saturation, as measured by pulse oximetry, should be monitored regularly on all post-arthroplasty patients. Hypoxemia should lead to a prompt and thorough medical workup. If an obvious explanation for the hypoxemia cannot be identified, the patient should undergo a multidetector CT scan to rule out a pulmonary embolus

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary patho-physiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury. It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma. Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m. 2. for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively. There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values. Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary pathophysiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury. It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma. Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m. 2. for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively. There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values. Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary pathophysiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury. It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma. Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m. 2. for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively. There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values. Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury

Introduction. Peak incidence of pulmonary embolism (PE) typically occurs weeks after total hip (THA) or knee (TKA) arthroplasty, long after hospital discharge. We investigated risk factors for acute PE occurring during index hospitalisation. Methods. Retrospective review of an IRB-approved database identified 329 arthroplasties performed by a single surgeon between 2002 and 2007 at two University teaching hospitals. Warfarin (goal INR 2.0) was standard venous thromboembolism prophylaxis. Results. There were 126 (38.6%) primary THA, 86 (26.1%) primary TKA and 117 (35.3%) revision arthroplasties. Seven patients (7/329; 2.1%) experienced clinically evident non-fatal pulmonary embolism, including 5 after TKA (5/128; 3.9%) and 2 after THA (2/194; 1.0%). In-hospital PE occurred in 4 (1.2%) patients (3 TKA, 1 THA) at a mean 2.7 days (range 2-4 days) after operation, compared with 3 symptomatic events (2 TKA, 1 THA) occurring after discharge (mean 19.3 days; range 8-27 days). Three of four patients suffering acute in-hospital PE were on pre-operative warfarin for chronic atrial fibrillation. Among all patients on pre-operative warfarin, 3 (12.5%) sustained an early PE, with a relative risk of 38.1 times that of controls not on chronic warfarin therapy (p=0.001). Body mass index greater than 30 kg/m2, a history of previous venous thromboembolism, coronary artery disease, ASA score, and type of operation were all found to not be associated with increased risk of in-hospital PE. Conclusion. Acute symptomatic in-hospital pulmonary embolism was correlated with chronic pre-operative warfarin anticoagulation. Compared to historical controls, time to PE was shorter in patients on chronic warfarin. Rebound hypercoagulability after discontinuation of chronic warfarin in preparation for total joint arthroplasty represents a greater hazard than excessive bleeding; we advocate bridging anticoagulation with LMWH in these patients

Background: Confusion occurs in up to 60% of patients following neck of femur fracture, delaying hospital discharge. We investigated venous – arterial circulation shunts (v-aCS) and the influence of cerebral embolism before and during surgery on subsequent cognitive function. Methods: Cerebral emboli were counted in 16 patients with an inter-trochanteric or Garden III/IV fracture by transcranial Doppler (TCD) monitoring over 1 hour pre-operatively and intra-operatively. A v-aCS was diagnosed when 1 or more microbubbles were detected in the middle cerebral artery by TCD following intravenous injection of a microbubble emulsion. Cognitive function was investigated by a battery of computerised tests preoperatively and at 5 days postoperatively. Results: Cerebral emboli were detected in 9 of 16 patients preoperatively (median 2, range 1–23) and in 10 patients during surgery (median 10, range 4 – 617). A v-aCS was associated with preoperative emboli in 9 patients (p=0.036, Fisher’s Exact) and intraoperative emboli in 10 patients (p=0.011, Fisher’s Exact). Cognitive function deteriorated following surgery only in patients with emboli, with the median (range) overall reaction times increasing from 3220ms (1926–5868) to 7493ms (4690–15992) [p=0.008]. The overall accuracy deteriorated from 2.57 to 2.37 (NS). Conclusion: Cerebral embolism is common following femoral neck fracture in patients with a v-aCS and was associated with a deterioration in cognitive function

Summary Statement. Pulmonary embolism (PE) after total knee arthroplasty can have a significant impact on patient outcomes and healthcare costs. Efforts to prevent or minimise PE over the last 10 years have not had a significant impact on its occurrence at the national level. Introduction. Pulmonary embolism (PE) is a rare but known potentially devastating complication of total knee arthroplasty (TKA). Significant healthcare resources and pharmaceutical research has been recently focused on preventing this complication but limited data exists regarding the early results of this great effort. The purpose of this study was to assess recent national trends in PE occurrence after TKA and evaluate patient outcomes related to this adverse event. Methods. International Classification of Disease - 9th Revision (ICD-9) procedure codes were used to search the National Hospital Discharge Survey (NHDS) for all patients admitted to US hospitals after primary TKA for each year between 2001 and 2010. ICD-9 diagnosis codes were then used to identify patients from this population who developed an acute PE during the same admission. Data regarding patient demographics, hospitalization length, discharge disposition, deep vein thrombosis, mortality, and hospital size/location were gathered from the NHDS. Trends were evaluated by linear regression with Pearson's correlation coefficient (r) and statistical comparisons were made using Student's t-test, z-test for proportions, and chi-square analysis with a significance level of 0.05. Results. 35,220 patients admitted for a primary TKA were identified. 159 (0.045%) of these patients developed an acute PE during the same admission. After adjusting for fluctuations in annual TKA performed, the development of PE after TKA demonstrated a weak negative correlation with time (r=0.17), insignificantly decreasing from an average rate of 0.049% between 2001–2005 to 0.041% between 2006–2010 (p=0.26). The size of the hospital was found to significantly impact the incidence of PE and primary TKA, with the lowest rate seen in hospitals under 100 beds (0.23%) and the highest rate seen in those with over 500 beds (0.65%, p=0.01). No significant differences in PE incidence were noted based on US region (p=0.38). The mean age of patients with PE was 67.7 years. This group included 54 men and 105 women. The non-PE group had a mean patient age that was insignificantly lower at 66.6 years (p=0.21) and included 12,450 men and 22,611 women. Gender was also not significantly different (p=0.68) between those with PE and those without PE. The number of medical co-morbidities was significantly higher in those with PE (mean 6.42 diagnoses) than those without PE (mean 4.89 diagnoses, p<0.01). Average hospitalization length also varied based on PE status, with significantly longer stays for those with PE (8.2 days, range 2–53) compared to those without PE (3.7 days, range 1–95, p<0.01). The rate of deep vein thrombosis was higher in the PE group (12.7%) versus the non-PE group (0.48%, p<0.01). Mortality was also significantly higher for the PE group (3.9%) compared to the non-PE group (0.09%, p<0.01). Discharge disposition did not significantly vary based on PE status, with 61.5% of PE and 64.0% of non-PE patients able to go directly home (p=0.59) after their inpatient stay. Discussion/Conclusion. This study demonstrates that PE can have a significant impact on patient outcomes and healthcare costs, with an associated 43-fold increase in mortality and a doubling of the inpatient admission duration. Additionally, although the risk of PE after primary TKA remains rare, it still persists. Efforts to prevent or minimise this complication over the last 10 years have not had a significant impact on its occurrence at the national level. This risk of PE appears to be greatest in patients with multiple medical co-morbidities and established DVTs. Interestingly, the PE rate also demonstrated variability based on hospital size. The reasons for this are not clear, but we suspect larger hospitals are more likely to be tertiary-care centers and thus care for more medically-complex patients

Fatal pulmonary embolism (PE) after total hip replacement (THR) is a major concern to all orthopaedic surgeons. Our intention was to ascertain death rates and deaths due to PE following total hip replacement where chemical thromboprophylaxis was not used routinely. We determined retrospectively, the postoperative mortality and fatal pulmonary embolism rates in 1671 consecutive primary total hop replacements in 1547 patients performed as staged procedures between January 1997 and April 2000 at an orthopaedic hospital. The minimum follow-up period was six weeks period after surgery at an orthopaedic hospital. Patients were traced by questionnaires, outpatient appointments and by telephone. Post-mortem records were used to verify cause of death. Follow-up was 100%. The death rate from PE was 0. 12% (CI 0. 03% – 0. 44%) and the all-cause mortality rate was 0. 36% (CI 0. 16% – 0. 78%). All deaths were within the first 10 days during the initial hospital stay. The patient mortality was compared with the population mortality for England and Wales, using standardised mortality ratios (SMRs). The SMR for both sexes combined was 0. 81. We observed a lower mortality in females (SMR=0. 43) but a higher mortality in males (SMR=1. 44) during the first 42 postoperative days compared to the general population. Fatal PE after THR without routine chemical thromboprophylaxis is very uncommon. The death rate in patients undergoing THR appears to be lower than that in the general population

Introduction:. Although the risk of pulmonary embolism (PE) or other embolic events associated with total joint arthroplasty have been recorded for some time, to date no direct means of these events in human arthroplasty have reported. This prospective study was designed to clarify the pathophysiologic mechanism of PE after total knee arthroplasty (TKA). Methods:. Nine patients fulfilling the following selection criteria were included in this prospective study: diagnosis of osteoarthosis, age 60 to 75 years, cemented primary TKA. All patients had a baseline pulmonary perfusion scan 2 days prior to the surgery. TKA was performed in the standard manner under general anesthesia. Monitoring of the heart chambers during the course of the TKA was performed using a 5 MHz ultrasonic transducer placed into the esophagus. The 4-chamber view plane of the heart was then imaged using a 2-dimensional echocardiography. A tip of the catheter inserted from the contralateral femoral vein was also placed in the inferior vena cava to harvest the venous blood flowed from the suffered lower extremity before and after tourniquet release. All patients had pulmonary perfusion scans 3 hours after TKA and on the 21st postoperative day. The ventilation-perfusion scan was compared with the baseline perfusion scan. Results:. No symptomatic PE were identified. Using transesophageal echocardiographic monitoring, the heaviest flow of embolic particles in the right heart was observed 2 seconds after tourniquet release and lasted approximately 30 seconds. By squeezing the calf muscle, the heavy flow of embolic particles was again observed. The venous blood harvested through the catheter after tourniquet release had fat droplets and white coagula. All of patients had pulmonary perfusion defects 3 hours after TKA, but no pulmonary perfusion defects on the 21st postoperative day. Discussion and Conclusions:. Substantial amounts of embolic materials were seen in the right heart using transesophageal echocardiography in patients operated in the standard manner. It was demonstrated that these embolic materials consisted of fat droplets and white coagula. We also demonstrated that many embolic materials for PE and/or DVT originated in the calf. All of patients had pulmonary perfusion defects just after TKA. It was concluded that all of the patients who underwent TKA had asymptomatic PE just after the surgery. Therefore, all of the patients have a possibility of symptomatic PE just after TKA